Rodney Rothstein

Columbia University


Election Year: 2015
Primary Section: 26, Genetics
Secondary Section: 21, Biochemistry
Membership Type: Member

Biosketch

Rodney Rothstein is a geneticist recognized for his work on genome stability. He is known particularly for his studies on DNA double-strand break repair and the development of methods to edit genomes. Using these tools, he isolated genes important for the maintenance of genome integrity and created strains to study in vivo imaging to reveal cellular responses to DNA damage. Rothstein was born in Seattle, WA in 1947 and grew up in the Chicago metropolitan area. He graduated from the University of Illinois, Chicago with a degree in biology (1969) and from the University of Chicago (1975) with a PhD in Genetics followed by post-doctoral studies at the University of Rochester and Cornell University, Ithaca, NY. He was a faculty member at UMDNJ in Newark (1979) before joining the faculty of Columbia University Medical Center in 1984. He received the Novitski prize from the Genetics Society of America (2009) and was awarded Doctor Honoris Causa in Medicine from Umeå University, Sweden (2012). He is a fellow of the American Society for Microbiology (2007), American Association for the Advancement of Science (2008) and the American Academy of Arts and Sciences (2011) and he is a member of the National Academy of Sciences.

Research Interests

Rodney Rothstein's laboratory uses yeast as a model organism to study genome stability, DNA repair and recombination. He pioneered the use of recombination to alter genomes and used these methods to isolate novel genes involved in the maintenance of genome stability. His “one-step” gene disruption method led directly to the “knockout” technology used in many organisms to exploit recombination to either remove or insert DNA sequences into specific genomic positions. His laboratory discovered many conserved genes affecting the control of genome stability, including Top3, a novel type I topoisomerase and Sgs1, a DNA helicase, mutation of its human homologues (Blm, Wrn and Rts) cause cancer predisposition and/or premature aging. By combining genetics and cell biology, his lab studies the choreography of the DNA damage response in living cells. They showed that recombination foci assemble at chromosome breaks and act as repair centers capable of repairing more than one DSB. They also found that chromosomal loci increase their mobility in response to DNA damage. They developed tools to screen for the ensuing genetic interactions caused by gene overexpression. They are using this approach to gain insight into the pathways that are disrupted by the common amplicons found in cancer cells.

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